|Recombinant Rat TNFRSF11A protein (Catalog#80160-R08H)|
|0.2 μm filtered solution in PBS with 5% trehalose|
|Produced in rabbits immunized with purified, recombinant Rat TNFRSF11A (rR TNFRSF11A; Catalog#80160-R08H; XP_573424.2; Met1-Pro213). Total IgG was purified by Protein A affinity chromatography.|
ELISA: 0.5-1 μg/mL
This antibody can be used at 0.5-1 μg/mL with the appropriate secondary reagents to detect Rat TNFRSF11A. The detection limit for Rat TNFRSF11A is approximately ≤ 0.039 ng/well.
Anti-Histone H3 rabbit monoclonal antibody at 1:200 dilution
Lane A: NIH3T3 Whole Cell Lysate
Lane B: Hela Whole Cell Lysate
Lysates/proteins at 30 μg per lane.
Goat Anti-Rabbit IgG (H+L)/HRP at 1/10000 dilution.
Developed using the ECL technique.
Performed under reducing conditions.
Predicted band size:15 kDa
Observed band size:17 kDa
TNFRSF11A is a member of the TNF-receptor superfamily. In mouse, it is also known as CD265. TNFRSF11A contains 4 TNFR-Cys repeats and is widely expressed with high levels in skeletal muscle, thymus, liver, colon, small intestine and adrenal gland. It is an essential mediator for osteoclast and lymph node development. TNFRSF11A and its ligand are important regulators of the interaction between T cells and dendritic cells. It can interact with various TRAF family proteins, through which this receptor induces the activation of NF-kappa B and MAPK8/JNK. Defects in TNFRSF11A can cause familial expansile osteolysis (FEO). FEO is a rare autosomal dominant bone disorder characterized by focal areas of increased bone remodeling. Defects in TNFRSF11A also can cause Paget disease of bone type 2 (PDB2). PDB2 is a bone-remodeling disorder with clinical similarities to FEO. Defects in TNFRSF11A are the cause of osteopetrosis autosomal recessive type 7 which characterized by abnormally dense bone, due to defective resorption of immature bone.